Prof. Dr. Teruna J. Siahaan
Aya and Takeru Higuchi Distinguished Professor,Department of Pharmaceutical Chemistry, School of Pharmacy, KU
University of Kansas, USA
Prof. Dr. Teruna Siahaan is the Aya & Takeru Higuchi Distinguished Professor of Pharmaceutical Chemistry at The University of Kansas (KU) and a Fellow of the American Association of Pharmaceutical Scientists (AAPS). His research is focused on improving drug delivery to the brain and immune cells; he published 200 papers, obtained 12 patents, and edited two books. He serves as the Director, Center for Global Health, School of Pharmacy, KU; Associate Chair, Department of Pharmaceutical Chemistry; and the Executive Board of Directors the Globalization Pharmaceutics Education Network (GPEN) Organization. He has received several honors and awards, including Self Faculty Scholar, KU; Pfizer Research Scholar Award; 2013 Mentor of the Year, KU; and 2014 PhRMA Foundation Award for Excellence in Pharmaceutics.
Prof. Dr. Teruna J. Siahaan’s research interests are in the utilization and modulation of cell adhesion molecules on the cell surface for enhancing drug permeation through the intestinal mucosa and blood-brain barrier (BBB) and for targeted drug delivery to a specific immune cell type for controlling autoimmune diseases. Dr. Siahaan’s group is using cadherin peptides to enhance permeation of large hydrophilic molecules (i.e., peptides and proteins) through the intestinal mucosa and BBB. The hypothesis is that E-cadherin peptides modulate the E-cadherin interactions at the intercellular junctions to create larger openings that will allow paracellular permeation of large hydrophilic molecules (e.g., peptides and proteins). His group is also using peptides derived from cell adhesion molecules (i.e., ICAM-1 and LFA-1) to target drugs to leukocytes and vascular endothelial cells in inflammatory and autoimmune diseases (i.e., rheumatoid arthritis). Cell adhesion peptides and proteins are being used to target antigenic peptides in bifunctional peptide inhibitor (BPI) and I-domain antigen conjugate (IDAC) to block the formation of the immunological synapse at the interface between T cells and antigen-presenting cells (APC). BPI and IDAC molecules have been shown to suppress autoimmune diseases in models for multiple sclerosis (MS), type-1 diabetes (T1D), and rheumatoid arthritis (RA).